GLUTATHIONE INFLUENCE ON BIOCHEMICAL INDICES OF BLOOD SERUM IN EXPERIMENTAL NEPHROPATHY
DOI:
https://doi.org/10.11603/mcch.2410-681X.2018.v0.i3.9552Keywords:
nephropathy, creatinine, glutathione, folic acidAbstract
Introduction. Kidney disease is one of the most common problems of modern medicine.
The aim of the study – to determine the effect of glutathione on the change in biochemical findings of blood under conditions of experimental nephropathy.
Research Methods. Experiment was carried out on 90 male albino rats with the body weight of 0.16–0.18 kg. The animals were introduced a single intraperitoneal dose of folic acid (200 or 50 mg/kg) for modeling nephropathy. Glutathione was introduced intragastrically (100 mg/kg) during 3 and 7 days after intoxication with folic acid. The concentration of creatinine, urea, albumin, total protein, activities of γ-glutamyltranspeptidase activity and alanylaminotranspeptidase weredetermined.
Results and Discussion. Under conditions of nephropathy the urea content increase by 27 % as compared with the control group on the third and by 15 % on the seventh day of the experiment was observed. The introduction of glutathione contributed to the normalization of the content of urea in the blood. An increase in the level of serum creatinine in rats with nephropathy (by using folic acid at a dose of 200 mg/kg) in 1.5 times in comparison with the control group was observed. On the seventh day the level of creatinine increased by 17 %. In the group of animals where nephropathy was caused by folic acid at a dose of 250 mg/kg, on the third day of the experiment the creatinine concentration increased 2.4 times and by 30 % on the seventh day of the study as compared with the control. Seven-day glutathione influence equates the creatinine values of experimental animals with those of the intact group.
Conclusions. Glutathione shows nephroprotective properties confirmed by a decrease in the manifestations of nephrotic syndrome and improvement of the functional parameters of the kidneys. The content of creatinine depends on the concentration of the toxicant. It can be used to diagnose the kidney condition and confirm the model of nephropathy.
References
Forman, H.J., Zhang, H., & Rinna, A. (2010). Glutathione: Overview of its protective roles, measurement, and biosynthesis. – Mol. Aspects Med., 30 (1-2), 1–12.
Vivancos, PD., Wolff, T., & Markovic, J. (2010). A nuclear glutathione cycle within the cell cycle. Biochem. J., 431, 169-178.
Lu, SC. Regulation of glutathione synthesis. (2009). Mol. Aspects Med., 30, 42-59.
Park, E.Y., Shimura, N., & Konishi, T. (2014). Increase in the protein-bound form of glutathione in human blood after the oral administration of glutathione. J. Agric. Food Chem., 62 (26), 6183-6189.
Burtis, C.A., Ashwood, E.R., & Bruns, D.E. (2012). Textbook of Clinical Chemistry and Molecular Diagnosis. USA: Elsevier.
Chevalier, R.L. (2006). Obstructive nephropathy: towards biomarker discovery and gene therapy. Nat. Clin. Pract. Nephrol., 2, 157-168.
Hannemann, A. (2011). Age- and sex-specific reference limits for creatinine, cystatin C and the estimated glomerular filtration rate. Clin. Chem. Lab. Med., 50, 919-926.
Bocedi, A. (2016). Biomarkers in kidney disease. Springer Science & Business Media: Dordrecht, 577-598.
Gupta, A., Puri, V., Sharma R., Puri S. (2012). Folic acid induces acute renal failure (ARF) by enhancing renal prooxidant state. Experimental and Toxicologic Pathology, 64 (3), 225-232.
Gozhenko, A.I. (2006). Patogenez toksicheskikh nefropatiy [Pathogenesis of toxic neuropathies]. Aktualnyye problemy transportnoy meditsiny – Actual Problems of Transport Medicine, 4 (2), 9-15 [in Russian].
